Some nice behind the scenes details on the working session not covered at the symposium.

Davis has began filtering substances out of ME/CFS patients’ plasma in an attempt to isolate the offending factor. (Note that the problem could also be a missing factor – something missing in ME/CFS patients’ blood.) The first stab indicated that the substance or compound was likely a large molecule; the next that it may be an antibody or something attached to an antibody. That’s an intriguing finding given Mark Davis’ belief that ME/CFS is probably an autoimmune disease.

In order to get as many minds as possible working on ME/CFS Ron Davis has promised to open up his data and that’s going to happen. Raeka reported that a web-based data platform for analysis and visualization of these datasets is going to be rolled out soon.

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@mariovitali is this data something you could incorporate into your machine learning algorithm?

Doctor Alert! – During a break Alan and his wife, Kathleen Light, made a plug for rapamycin, (rapamune) case reports in ME/CFS. Several accounts of ME/CFS patients doing better on Rapamune have been making the rounds. The Light’s dearly want those case studies to get written up in the scientific literature. That’s all they need to provide the foundation they need to get Rapamune studied in ME/CFS

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I've emailed Dr Light the name of a doctor currently using it for ME

Thought this was noteworthy as well...

The results of the Bergquist Lyme/ME/CFS spinal fluid study were fascinating – it found different protein signatures in the spinal fluid of people who’ve been treated for Lyme disease and ME/CFS. That suggests that these two diseases or conditions, which look so similar and which some people think are the same, are probably quite different; pTLD is not a subset of ME/CFS or vice versa

Thus far the massive project has identified 14 genes that are possibly implicated in ME/CFS, including one highly suspect gene that had damaging mutations in every severe patient but not in a single healthy control.

Davis, as usual, expressed caution; that gene – which affects serotonin processing and regulatory T-cells – could be associated with severity but may not be causing ME/CFS; i.e. ME/CFS might simply be worse in people with these mutations. Either way, if the finding holds up, it’s a clue – an arrow pointing at an area of dysfunction.

Problems with that gene could conceivably make it difficult to halt the proliferation of T-cells – ultimately putting ME/CFS patients at risk for an autoimmune disease.

'Doctor Alert! – During a break Alan and his wife, Kathleen Light, made a plug for rapamycin, (rapamune) case reports in ME/CFS. Several accounts of ME/CFS patients doing better on Rapamune have been making the rounds. The Light’s dearly want those case studies to get written up in the scientific literature. That’s all they need to provide the foundation they need to get Rapamune studied in ME/CFS'

My friend is a microbioogist and she likes to use the term bug! it seems to cover most microbes, e.g. bacteria, bacteriophages, parasites and archaea. Bacteria is the most well-known but many things live in us.

FWIW I found the piece fascinating:

Blood has always been considered free from microbes, because bacteria don’t grow when it is put in a culture dish. But recent DNA sequencing methods reveal that each millilitre of blood in fact contains around 1000 bacterial cells.

These bacteria are usually dormant. But they can be revived when iron becomes available in the blood, and begin secreting lipopolysaccharides (LPS) – molecules on their cell walls that are recognised by the immune system and stimulate inflammation.

Their focus is on dormant microbes waking up and causing clotting. I imagine that's not all they could cause. There was an interesting thread the other day about people with curiously low blood iron. Could that be the body's attempt to keep these dormant bugs dormant?!

In no way i am trying to stop the excitement. I just believe that we have to be extremely cautious.

I am very concerned because 5 out of 6 people with CFS were found to have Liver fibrosis (stage 2 and greater) after taking a Fibroscan test. I am also very concerned because several patients of CFS got this syndrome after taking certain medications. We know that certain medications generate Oxidative Stress while being metabolised at the Liver.

Rapamycin has a lot of side effects. I am not saying that it shouldn't be tried, i am saying that caution is warranted here.

Ultimately we must find the source of the problem and not treating its symptoms.

Doctor Alert! – During a break Alan and his wife, Kathleen Light, made a plug for rapamycin, (rapamune) case reports in ME/CFS. Several accounts of ME/CFS patients doing better on Rapamune have been making the rounds. The Light’s dearly want those case studies to get written up in the scientific literature. That’s all they need to provide the foundation they need to get Rapamune studied in ME/CFS

@Cort, can patients who've been treated with rapamycin help with this by contacting their doctors and asking them to contact the Lights? Or writing to the Lights and asking them to contact their doctors? If so, you might want to start a new thread with that call to action. (You might want to check with the Lights first! )

I have been thinking for a long time whether I should write this or not. This is something that worries me very much, so I've decided to share my thoughts with you. I've tried to keep it as short as possible, because I don't want to take too much of your precious time.

I've been reading some of the great reports of the symposium. I think it's wonderful that Ron wants to share his data and that he wants to work together with anybody to solve this disease. I do however have my doubts about collaborating with professor doctor Kenny de Meirleir who was also present according to the reports.
It's not my intention to spread slander about him. I do, however, want to warn you that his way of working is questionable and he is not completely reliable. He doesn't disclose his conflicts of interest and they do exist. His statements made to colleagues (doctors, fellow-scientists) and patients are often incorrect, exaggerated, contradictory and even misleading.
I found out the hard way and I want to prevent this from happening to you. It is so important that Ron, the Stanford Group and OMF succeed.
Please be careful and be critical.

One of my big take-aways from this is that a bunch of researchers I didn't know about are on the case. How good is that!

For biologists this must be a bit like a gold rush. A whole disease lying in wait, ready to be uncovered. Hopefully we can keep recruiting more top minds (and their research budgets!) to the cause

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Unfortunately they don't have big or sometimes any research budgets for me/CFS. They do pilot studies or just do what they can with minimal funding. OMF has helped but Ron said at the symposium that the biggest block to progress is funding. That's why we are hoping their grant proposal for one of the NIH centers gets funded. Some of this research is included in that proposal. Cross your fingers and toes! It would be a wonderful thing to get these great scientists pulled into the field and attract more. Indeed, they are starting to realize what an interesting and urgent puzzle this is, and for them such things are fun! We need these people involved!

Found this article extremely interesting! Watched the 8 hour lifestream of the symposium but the article offers lots of additional information.

Didn't know that such a huge study is happening with Mike Snyder. Makes me so hopeful!

The ME/CFS study underway in his lab is huge – 10 families thoroughly investigated so far with many more to come and 175 non-familial cases of ME/CFS and 150 controls – all incorporated into a major multi-omics (genomics, metabolomics, microbiome, etc.) study (!!!).

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I just recently realized that infections can trigger several chronic diseases and that this is not ME/CFS-specific. Found this example with diabetes and how genes could be involved very interesting (but also over my head):

Jahanbani noted that different genetic variants might be leading to the same endpoints – a dysregulated immune system and metabolic impairment that popped up after some severe stressor, such as an infection.

She referenced how an infection appeared to flip a switch in one person which exposed a mutation in a gene which had been inactive before, which then resulted in that person coming down with Type II diabetes.

That’s a pretty apt model for ME/CFS and is exactly the kind of hypothesis they’re probably hoping to uncover; an infection or event that flips some sort of switch, which then turns on an inactive gene mutation or some other factor, which then results in ME/CFS.

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This gave me hope, too. A researcher who didn't know anything about ME/CFS, but read about it in a Stanford magazine and found it so exiting that he wanted to contribute. This is the worst part for me that no one seems to be interested in this stigmatized disease, I can literally see doctors shutting off their brains as soon as I mention the words ME/CFS ("It's only a syndrome, I'm tired too by the way, just do some exercise and let me treat patients with real diseases"). So that this is starting to change and ME/CFS is considered interesting (and with it its sufferers) is most important!

Phair’s story indicates why it’s important that we keep communicating, communicating, communicating about this disease. Phair had a friend with the disease, but didn’t know diddly about it or what he could contribute towards it until a piece on ME/CFS appeared in the Stanford alumni magazine.
He said “Without that story, I wouldn’t be here.” He contacted Laurel Crosby and has been volunteering with her and Ron about one day a week for the past year.

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They are searching participants for a new severely ill patients study:

Alert! Fereshtah is looking for nine more severely patients in the San Francisco Bay area (within an hour of Stanford) to fill up her intensive study of 20 severely ill patients and their families. Please contact her at fjahania@stanford.edu.

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Haven't read through the whole very long (and in English) article yet. But find this view behind the scenes amazing!

@Cort, can patients who've been treated with rapamycin help with this by contacting their doctors and asking them to contact the Lights? Or writing to the Lights and asking them to contact their doctors? If so, you might want to start a new thread with that call to action. (You might want to check with the Lights first! )

Found this article extremely interesting! Watched the 8 hour lifestream of the symposium but the article offers lots of additional information.

Didn't know that such a huge study is happening with Mike Snyder. Makes me so hopeful!

I just recently realized that infections can trigger several chronic diseases and that this is not ME/CFS-specific. Found this example with diabetes and how genes could be involved very interesting (but also over my head):

This gave me hope, too. A researcher who didn't know anything about ME/CFS, but read about it in a Stanford magazine and found it so exiting that he wanted to contribute. This is the worst part for me that no one seems to be interested in this stigmatized disease, I can literally see doctors shutting off their brains as soon as I mention the words ME/CFS ("It's only a syndrome, I'm tired too by the way, just do some exercise and let me treat patients with real diseases"). So that this is starting to change and ME/CFS is considered interesting (and with it its sufferers) is most important!

They are still searching participants for the severely ill patients study:

Haven't read through the whole very long (and in English) article yet. But find this view behind the scenes amazing!

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The Snyder study was the most exciting part of the Symposium. My jaw dropped when I learned how big it was...(Who knew?)